The transient receptor potential (TRP) family of ion channels are often found to be sensors of multiple chemical and physical stimuli (temperature, smell, taste and noxious chemicals). Particularly, the non-selective cation channel TRPA1 (transient receptor potential ankyrin-repeat 1), originally cloned as an ankyrin-like protein (Jaquemar et al 1999, J Biol Chem 274:7325-7333), is activated by multiple pungent and pro-algesic compounds (Bandell et al 2004, Neuron 41: 849-857). Recent reviews on TRPA1 as pharmaceutical target have been published by Rech et al. (Future Med. Chem. 2010: 843-838) and by Baraldi et al (J. Med. Chem. 2010, 5085-2107). TRPA1 is highly expressed in a subset of C-fiber nociceptors in the peripheral nerve system (Kobayashi et al 2005, J Comp Neurol 493(4):596-606). When activated TRPA1 permits the conduction of cations (primarily Ca2+ and Na+) from the extra cellular environment into the cell, thereby depolarizing the membrane potential and affecting calcium homeostasis in the primary afferents. Depolarization primary nerve terminals lead to action potential firing and consequently increased pain sensation and hyperalgesia in man and rodent experimental models (Jiang and Gebhart 1998, Pain 77(3):305-13; Cervero and Laird 1996, Pain 68(1):13-23). The pungent ingredient in mustard oil: allyl isothiocyanate (AITC), concentration dependently activates TRPA1 in vitro measured both on sodium current and calcium influx. Further, AITC also excites small diameter afferent fibers (Reeh 1986, Brain Res 384:42-50) and indeed topical application of AITC induces pain and hyperalgesia in man (Namer et al 2005, Neuroreport 16(9):955-959). Recently TRPA1 knock out (KO) mice were described to have lost AITC sensitivity and display severely impaired bradykinin pain response signalling (Kwan 2006, Neuron 50(2):277-289; Bautista 2006, Cell 124(6):1269-1282). Formalin, which is a mixture of methanol, water and formaldehyde is a widely used rodent model for evaluating analgesic compounds in vivo. TRPA1 is activated by formaldehyde in vitro and recently it was shown that TRPA1 KO mice almost have their response to formalin/formaldehyde abolished (McNamara et al 2007, Proc Natl Acad Sci USA 104(33):13525-13530). A Hydra Biosciences proprietary compound (HC030031) is a TRPA1 antagonist in vitro and has been shown to alleviate the formalin induced pain behaviour in a dose dependant way (McNamara 2007, Proc Natl Acad Sci USA 104(33):13525-13530 and WO2007/073505 A2). An Abbott proprietary compound (US 2009/0176883 and McGaraughty et al., Molecular Pain 2010 6:14) with in vitro effect on TRPA1 showed to have in vivo effect in a rat osteoarthritis pain model as well as a number of Glenmark proprietary compounds (US 2009/0325987) showed in several in vivo pain models. It has also been shown that a mutation in TRPA1 causes FEPS (“Familial Episodic Pain Syndrome”, Kremeyer et al, Neuron 2010, 66:671-680). It is therefore suggested that in vitro inhibition of the TRPA1 calcium and sodium influx will determine a compound's propensity to work as an analgesic in vivo. An object of the present invention is therefore to provide new, improved and useful analgesics.